PREOPERATIVE CARDIAC EVALUATION

FOR NONCARDIAC SURGERY (PART-1)

Moderator- Dr. Mamta Sharma

Presented by - Dr. Sudhanshu

INTRODUCTION
Preoperative risk assessment is an important
step in reducing perioperative morbidity and
mortality in patients undergoing non cardiac
surgery.
Successful perioperative evaluation is best
achieved
by
combining
an
integrated
multidisciplinary
approach
with
good
communication between the patient, primary
care physician, anesthesiologist, consultant,
and surgeon.

GOALS
Identify patients at risk through History, Physical
examination, & ECG
To Evaluate severity of underlying cardiac
disease, Perform specialized test only on High risk
Patients
Stratify the Extent of Risk & determine The need
for preop intervention to minimize the risk of
perioperative cardiac complications
The goal of appropriate preoperative evaluation and
therapy should be to not only improve immediate
periprocedural outcomes but also to improve long
term clinical outcome.

 Cornerstone of Preoperative cardiac

examination includesReview of History
Physical Examination
Diagnostic Tests
Knowledge of planned surgical
procedure

Eight Steps to the Best Possible Outcome

1.
2.
3.
4.
5.
6.
7.
8.

Assess the Patients Clinical Features

Evaluate Functional Status
Consider the Patients Surgery-Specific Risk
Decide if Further Noninvasive Evaluation Is
Needed
Decide When to Recommend Invasive
Evaluation
Optimize Medical Therapy
Perform Appropriate Perioperative Surveillance
Design Maximal Long-Term Therapy

History
Presence, severity & reversibility of Heart disease
Risk factorsAge
Hypertension
Diabetes Mellitus
Hyperlipidemia
Cigarette Smoking
Alcohol
Family History of heart disease- HOCM, Marfan
syndrome, Long Q-T syndrome

History Cont.

Chest pain
Shortness of breath
Ankle swelling/ peripheral oedema
Palpitations- sensation of the heart
beating in the chest
Syncope
Intermittent claudication

Chest Pain

Character of pain

Severity
Duration
Radiation

At rest or on exertion

Previous episodes

Relieving factors
Worse on taking a
deep breath
(pleuritic)
Worse on movement
Autonomic symptoms
Sweating
Nausea

Chest Pain
Type

Cause
Coronary stenosis (rarely
aortic stenosis,
hypertrophic
cardiomyopathy)

Characteristics
Precipitated by exertion,
eased by rest and/or
glyceryl trinitrate
Characteristic distribution

Myocardial infarction

Coronary occlusion

Similar sites to angina,

more severe, persists at
rest

Pericarditic pain

Pericarditis

Sharp, raw or stabbing

Varies with movement or
breathing

Aortic pain

Dissection of the aorta

Severe, sudden onset,

radiates to the back

Angina

Causes of Chest Pain

Cardiovascular
Angina

Stable
Unstable

Myocardial infarction
Aortic dissection
Myocarditis

Pleuropericardial
Pericarditis
Pleurisy
Pneumothorax

Gastrointestinal

Gastro-oesophageal
reflux
Oesophageal spasm

Chest wall
Coughing
Intercostal muscle
strain/myositis
Herpes zoster
Viral pleurodynia
Thoracic radiculopathy
Rib fracture
Rib tumour
Costochondritis

Dyspnoea
Unexpected awareness of breathing
At rest or on exertion
Quantify exercise tolerance (yards
walked, stairs climbed)
Orthopnoea - shortness of breath on
lying supine
Paroxysmal nocturnal dyspnoea

Causes of Dyspnoea

Cardiac

Left ventricular failure

Mitral valve disease
Cardiomyopathy
Pericardial effusion

Airways disease
COPD

Pulmonary vasculature
Pulmonary embolism
Pulmonary hypertension

Pneumonia
Pulmonary fibrosis
Tumour
Pneumothorax

Chest wall

Chronic bronchitis
Emphysema

Asthma
Bronchiectasis
Cystic fibrosis

Parenchymal disease

Pleural effusion
Rib fracture
Kyphoscoliosis
Neuromuscular

Other

Anaemia
Acidosis
Psychogenic

New York Heart Association classification

of heart failure symptom severity
Class I

No limitations. Ordinary physical activity does not cause undue fatigue,

dyspnoea or palpitation (asymptomatic left ventricular dysfunction)

Class II

Slight limitation of physical activity. Such patients are comfortable at rest.

Ordinary physical activity results in fatigue, palpitation, dyspnoea or angina
pectoris (symptomatically 'mild' heart failure)

Class III

Marked limitation of physical activity. Less than ordinary physical activity will
lead to symptoms (symptomatically 'moderate' heart failure)

Class IV

Symptoms of congestive cardiac failure are present even at rest. With any
physical activity increased discomfort is experienced (symptomatically
'severe' heart failure)

PERIPHERAL OEDEMA
Unilateral or bilateral
legs
Pitting/non-pitting
Cardiac causes Congestive cardiac
failure
Right ventricular failure
Cor pulmonale
Constrictive pericarditis

Drugs
Calcium channel
blockers

Other
Cirrhosis
Nephrotic syndrome
Protein-losing
enteropathy
Deep vein thrombosis
Hypothyroidism
Lymphoedema

Palpitations

Unexpected awareness
of heartbeat
Ask about The mode of onset and
termination
Specific triggers of
exercise, alcohol,
caffeine
Frequency
Duration of attacks
Rhythm (ask patient to
tap out).

Causes
Sinus tachycardia
Ventricular
extrasystoles
Atrial fibrillation
Atrial flutter
Supraventricular
tachycardia
Ventricular
tachycardia

Syncope
Transient loss of consciousness due to
cerebral hypo-perfusion -Left ventricular
outflow obstruction, postural
hypotension, arrhythmias
What was the patient doing at the time?
Standing up suddenly (postural hypotension)
Coughing
Prodromal symptoms
Abnormal movements (epilepsy)
Sensation of room spinning (vertigo)

Intermittent Claudication
Pain in one or both calves, thighs or
buttocks
Brought on by walking a certain
distance (claudication distance)
Worse on walking uphill
Relieved by rest
Suggests peripheral vascular disease

Past Medical History

Rheumatic fever
Cong Heart disease- episode of cyanotic/
tet spells
Valvular Heart disease
Previous cardiac investigations
Previous myocardial infarction
Coronary angioplasty + stent insertion
Coronary artery bypass grafting
Pacemaker insertion

Non cardiac symptoms

System
Symptom
Central nervous system Stroke

Cause
Cerebral embolism

Endocarditis
Hypertension

Gastrointestinal

Renal

Jaundice

Liver congestion secondary to heart

failure

Abdominal pain

Mesenteric embolism

Oliguria

Heart failure

Medications
Anti-anginal agents

Use of sublingual nitrate spray

Antihypertensive agents
Anti-arrhythmics
Statins
Platelet inhibitors, e.g., Aspirin
Anticoagulants, e.g., Warfarin

Allergies

Social History
Occupation
e.g., train driver, long distance truck
driver

Smoking
Number of pack years

Alcohol intake
Stairs at home

Family History
Ischaemic heart disease
Angina
MI
CABG

Hypertrophic obstructive
cardiomyopathy
Dilated cardiomyopathy

Assessment of Functional
Capacity
The metabolic equivalent, or MET, is defined as the
ratio of a person's working metabolic rate relative to the
resting metabolic rate.
One MET represents the oxygen consumption of a
resting adult (3.5 ml/kg/min).
In the Revised cardiac risk index by Lee et al
functional status was not independently associated with
risk.
If patients reduce exertion because of cardiac symptoms
but still meet a 4-MET threshold, clinicians will
underestimate risk.
Conversely, non cardiac functional limitations (e.g., knee
or back pain) may falsely overestimate cardiac risk.

Dukes Activity Status Index

1 MET

4 METs

Can you take care of

yourself?

4 METs

Climb a flight of stairs or

walk up a hill?

Eat, dress, or use the

toilet?

Walk on level ground at 4

mph or 6.4 km/hr?

Walk indoors around

the house?

Run a short distance?

Walk a block or two on

level ground at 2-3
mph or 3.2-4.8 km/hr?

Do heavy work around the

house, such as scrubbing
floors or lifting or moving
heavy furniture?

Do light work around

the house, such as
dusting or washing
dishes?

Participate in moderate
recreational activities such
as playing golf, bowling,
dancing, playing doubles
tennis, or throwing a
baseball or football?
10 METs

Participate in strenuous
sports such as swimming,
singles tennis, football,
basketball or skiing?

Physical Examination
General-pallor,
cyanosis
Hands
Pulse
Blood pressure
Face
Neck
Jugular venous
pressure

Pre-cardium

Inspection
Palpation
Percussion
Auscultation

Back
Abdomen
Lower limbs

Examination - General

Position patient at 45 degrees

Respiratory rate
Cachexia
Marfans syndrome
Downs syndrome

Examination - Hands
Clubbing
Splinter haemorrhages (infective
endocarditis)
Oslers nodes (tender)
Janeway lesions (non-tender)
Xanthomata (Hyperlipidaemia)

Splinter
Haemorrhages
Clubbing

Examination - Pulse
Radial artery
Rate (normal = 60100)
Bradycardia (<60)
Tachycardia (>100)

Rhythm
Regular
Irregular

Radiofemoral delay
(coarctation of the
aorta)

Character and volume,

assessed from carotid
artery
Collapsing pulse (aortic
regurgitation)
Pulsus alternans (left
ventricular failure)
Pulse deficit (atrial
fibrillation)

Peripheral Pulses

Dorsalis pedis
pulse

Posterior tibial
pulse

Examination - Blood
Pressure
Systolic/diastolic
pressure
Normal <140/90
mmHg (lower in
diabetes)
Use larger cuff width
for large arms

Deflate at 4 mmHg/s
Difference between
arms of <10 mmHg
Pulsus paradoxus =
exaggerated
reduction in BP with
inspiration (>10
mmHg)
Postural hypotension

Examination Face and

Neck

Jaundice
Xanthelasmata
Corneal arcus
Malar flush (mitral
stenosis)
High arched palate
(Marfans syndrome)
Dental caries
(infective
endocarditis)

Central cyanosis
Carotid pulse
character

Slow rising (AS)

Bisferiens (AS + AR)
Collapsing (AR)
Alternans (LVF)
Jerky (HOCM)

Carotid bruit

Eye signs in
Hyperlipidaemia

CORNEAL
ARCUS

XANTHELASMATA

JVP

Jugular Venous Pressure

Patient at 45 degrees
Good lighting
Internal jugular vein
Reflects right atrial
pressure
Zero point = sternal
angle
Visible but not palpable
Complex wave form (a,
c, v waves)
Decreases on inspiration

Hepatojugular reflux
Abnormal if >3 cm above
zero point:

RV failure
RV infarct
Tricuspid stenosis
Tricuspid regurgitation
Pericardial effusion
SVC obstruction
Fluid overload

Jugular venous pressure in a healthy subject.(A)

Supine: jugular vein distended, pulsation not visible.
(B) Reclining at 45: point of transition between
distended and collapsed vein can usually be seen to
pulsate just above the clavicle. (C) Upright: upper part
of vein collapsed and transition point obscured

 jugular venous pressure.

Form of the venous pulse wave
tracing from the internal jugular
vein:
a = atrial systole;
c = transmitted pulsation of
carotid artery at onset of
ventricular systole;
v = peak pressure in right atrium
immediately prior to opening of
tricuspid valve;
a - x = descent, due to atrial
relaxation;
v - y = descent at
commencement of ventricular
filling.

Abnormalities of the jugular venous pulse

Heart failure

Elevation, sustained
abdominojugular reflux

Pulmonary embolism

Elevation

Pericardial effusion

Elevation, prominent 'y'

descent

Pericardial constriction

Elevation. Kssmaul's
sign

Superior vena caval

obstruction

Elevation, loss of pulsation

Atrial fibrillation

Absent 'a' waves

Tricuspid stenosis

Giant 'a' waves

Tricuspid regurgitation

Giant 'v' waves

Complete heart block

'Cannon' waves

Precordium - Inspection
Scars
Median sternotomy
CABG
Valve replacement

Lateral thoracotomy
Infraclavicular
(pacemaker)

Pectus excavatum
Pacemaker box
Apical impulse

Sternotomy
scar

Pectus
excavatum

Precordium - Palpation

Apex beat-Lt 5th ICS

medial to the midclavicular
line
Location
Character

Heaving
Thrusting
Double
Tapping
Paradoxical

Left parasternal heave

Thrills (palpable murmurs)
Systolic
Diastolic

Palpable P2 (pulmonary
hypertension)
Pacemaker box

Precordium Auscultation
Heart Sounds
Bell low pitched
sounds
Diaphragm high
pitched sounds
Mitral Tricuspid
Pulmonary
Aortic areas
S1 (first heart
sound)
S2 Splitting (A2,
P2)

Normal Heart Sounds

Precordium Auscultation
Murmurs
Timing of murmur
Systolic
Diastolic
Continuous

Site of maximal
intensity
Loudness
Grades I-VI
Thrill

Pitch
Radiation
Dynamic
manoeuvres
Respiration
Left-sided on exp.
Right-sided on
insp.

Valsalva
Squatting

Grading of Murmur
I. Heard by an expert in optimum
conditions
II. Heard by a non-expert in optimum
conditions
III. Easily heard; no thrill
IV. A loud murmur, with a thrill
V. Very loud, often heard over wide
area, with thrill
VI. Extremely loud, heard without
stethoscope

Heart Murmurs
Diastolic
Systolic
Pansystolic
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect

Ejection systolic

Aortic stenosis
Pulmonary stenosis
HOCM
Atrial septal defect

Late systolic
Mitral valve prolapse

Early diastolic
Aortic regurgitation
Pulmonary
regurgitation

Mid-diastolic
Mitral stenosis
Tricuspid stenosis
Atrial myxoma

Continuous
Patent ductus arteriosus
Arteriovenous fistula

Pericardial friction
rub

Examination Back
Percuss and auscultate lung bases
Left ventricular failure
Pleural effusion

Sacral pitting oedema

Right heart failure

Examination - Abdomen

Tender hepatomegaly
Pulsatile liver (tricuspid regurgitation)
Ascites
Spleenomegaly
Abdominal aortic aneurysm

Examination Lower Limbs

Peripheral oedema
Pitting/non-pitting
Upper level

Achilles tendon
xanthomata
Capillary return
Trophic skin changes

Palpate arteries

Femoral
Popliteal
Posterior tibial
Dorsalis pedis
Buergers test
(peripheral vascular
disease)

Examination - Other
Urinalysis
Haematuria
(infective
endocarditis)

Fundi
Hypertensive
retinopathy
Roth spots
(infective
endocarditis)

Temperature chart
Infective

Investigation
RoutineCXR
ECG
Specialized testsNon invasive tests
Invasive Tests

Chest X-RAY
Non invasive method of estimating cardiac
function
Preoperative screening tool
Provides useful information in both coronary
artery disease and valvular heart disease
PA and Lateral view
Rt border-SVC and RA
Lt Border-Aorta, Main Pulmonary artery, Lt
Atrial appendages, Anterolateral Border of LV

CHEST X RAY.

A- AIRWAY
B-BONES
C-CARDIAC SILHOUTTE
D-DIAPHRAGM
E-EDGE OF HEART
AND EXTERNAL SOFT
TISSUE
F- FIELDS
G- GASTRIC BUBBLE
H-HILA

NORMAL ANATOMY

Normal CXR

Normal posteroanterior chest X-ray.Note vertebral

outlines just seen through the heart shadow. A/B - the
cardiothoracic ratio should be < 50%.

Changes in different cardiac

diseases
RA enlargement can be detected by broadening of right
heart contour
LA enlargement leads to displacement of LA appendage
laterally and lt. Bronchus upwards
In massive LA enlargements rt border of LA may overlap rt
heart border DOUBLE HEART SHADOW
Regurgitant lesion- Long axis is elongated with downward
and leftward displacement of apex
CAD- both long axis short axis enlargment- globular shaped
heart
RV enlargement Lat view- Obliteration of retrosternal
space

CHF
DIFFUSE B/L
ALVEOLAR OPACITIES
HAZZINESS OF
VASCULAR MARKINGS
CARDIOMEGALYmaximum diameter is
more than half the
internal trans-thoracic
diameter
(cardiothoracic ratio)
in inspiration PA view

What do the arrows

indicate?

Kerley B
Lines

Short (1 -2 cm)
white lines at
the lung bases,
perpendicular to
the pleural
surface
representing
distended
interlobular
septa

Pulmonary Oedema

Normal Chest
Radiograph

Pulmonary
Oedema

Pericardial effusion

Cardiomegaly
Narrow pedicle
Olegemic lungs
Broad based heart
Margins clear

PLEURAL EFFUSION
75ml of fluid is
needed to
obliterate the
posterior cp angle
Meniscus sign
Lamellar effusions
may spare the cp
angle
Ultrasound is more
valuable

Mitral stenosis
Bulging on rt sidedouble cardiac
shadow
Prominence of LA
appendage,
straightening of left
heart border
Elevation of lt main
bronchus

TOF

ECG
In standard 12 lead ECG Look for- rate, rhythm,
axis, abnormality of p waves, QRS complex, t
wave, ST segment, PR, QT & R-R intervals
Detect MI
ST-T changes
Q Waves
Chamber enlargementVoltage, strain criteria
Arrhythmias- conduction abnormality

ECG
Anteroseptal- V1-V4
Anterolateral- V4-V6
Inferior leads:
II,III,aVf
Post. Wall: Reciprocal
Changes in V1-V4

Left axis Deviation

LVH
voltage criteria for LVH :
The sumof the S wave in v1 or
v2, PLUS the R wave in v5 or
635mm, OR,
Thesum of the deepest S wave +
the tallest R wave > 40m
Anysingle, R or S, wavein leads v1v645mm
LVH+hypertension or aortic stenosis,
a 'strain pattern' is often seen:
ST depression + flipped asymmetric
T wave
ST elevation + upright asymmetric T
wave
The strain pattern is greatest in the
lead with the tallest/deepest QRS
complex.

Acute Anteroseptal MI

Indications for preoperative

cardiac testing :
1. Patients with intermediate clinical
predictors.
2. Prognostic assessment of patients
undergoing initial evaluation for
suspected or proven CAD.
3. Evaluation of patients with change in
clinical
status.
4. Evaluation of adequacy of medical

Noninvasive tests
1.Resting tests
Ambulatory ECG monitoring.
Resting ECHO.
2.Trans esophageal echocardiography
3.Exercise stress test.
4.Pharmecological stress test
DSE.
DTS.
5.Nuclear imaging

Ambulatory Electrocardiography (24

h Holter monitoring)
Continuous ECG monitoring of ambulatory pt by tape
recorder (holter monitoring)
Used to evaluate cardiac arrhythmias, antiarrhythmic
drug therapy and severity frequency of ischemic
episode
Correlation of symptom( palpitation dizziness
syncope) are often most valuable result of recording
Silent ischemic episode are frequent finding
Preoperative occurrence of frequent ischemic
episodes correlates well with intraoperative & postop.
Ischemia.
Relatively inexpensive

24-hour ambulatory ECG recording, showing

complete heart block.Arrows indicate visible P waves;
at times these are masked by the QRS complex or T wave

Resting Echocardiography
Simple and inexpensive
Indication- Detection of impaired LV function,
valvular heart disease
InformationRWMA- Types-Hypo/akinesia, dyskinesia
Location-ant, septal, lat, inf, post.
Ejection Fraction
Chamber Enlargement
Valve morphology,
Diagnosis of cong. Heart disease

TEE
Provide Clearer images- heart rests directly upon the
esophagus leaving only millimeters that the ultrasound
beam has to travel. This reduces the attenuation of the
ultrasound signal, generating a stronger return signal,
ultimately enhancing image and Doppler quality.
Valuable in diagnosis of MI, VHD complicated cong heart
disease , and assessment of ventricular function (Morbid
Obese pt)
very high sensitivity for locating a blood clot inside the
left atrium
Disadvantage- may require anaesthesia, fasting of pt
Esophageal perforation cases has been reported

Exercise Stress
Testing(Treadmill)
Physiology-Mean

arterial
Pressure
Increases despite significant decrease in SVR
Due to increase in cardiac output ( Upto 4X)
HR increase by upto 300%
Stroke volume increase by upto 20%
Increase in Oxygen consumption is meet
mainly
by
increasing
blood
flow
(vasodilatation by exercise and metabolites)
Coronary vascular reserve play imp role in
ischemic heart response to exercise

Bruce Treadmill protocols

Consists of 3 min stages having different grade and speed
Stage 1= 1.7mph & 10% grade
Sign and symptom of ischemia, arrythmias and pump dysfunction
measured
Principal indicator of ischemia- ST segment deviation
3 types of responseI. ST segment depression during exercise, normal in post exercise
period
II. ST segment depression during exercise, worsening in recovery
period
III. ST segment elevation
.Accepted criteria- elevation of 1.5 mm or more
.Changes in T wave, R wave, hypotension chest pain arrhythmias
also considered.

Information by TMT
Peak heart Rate, Systolic BP & double product
METS& % of Heart rate achieved
ECG changes, symptoms, or arrhythmias
occurring during test & at recovery period
A pt with symptoms or arrhythmias at a lower
workload is at increase risk as compared with
a patient able to reach a higher MET
thresholds.
Double pressure product must remain
below the ischemic thresholds.

Limitation & Interpretation

of TMT
Only Half of the pt achieve peak HR>75% of his age
predicted maximum
A ve test in a pt. who achieves target HR BP
product is usually associated with low risk for
perioperative cardiac complication
Ischemia induced by low level exercise indicates high
risk
Failure to reach the target HR makes the test
inadequate for excluding MI unless a normal workload
is achieved despite lower HR and such pt. are at
higher risk for perioperative complication.
PPV=18% NPV=97%

Dipyridamole-thallium
scintigraphy
Dipyridamole- Powerful coronary dilator
MOA- preventing uptake and degradation of
adenosine(auto-regulate coronary flow in
response to ischemia)
Distribute blood to normal coronary and reduce blood
flow Distal to ischemia (coronary steal phenomena
)
Thallium demonstrate myocardium at risk
Theophylline caffine avoided before test( antagonist)
S/E- Bronchospasm, chest pain, headache
Reversed by iv Aminophylline

Dobutamine stress
echocardiography
stress testing should be limited to patients
with suspicion of a myocardium at risk of
ischemia
MOA- Dobutamine increase myocardial
oxygen demand , increase HR, and inotropy
Detect new or worsened RWMA & severity
Baseline ejection fraction
Avoided in pt with- Arrythmias, marked
Hyper/Hypotension, critical AS

Nuclear imaging
Myocardial perfusion scan using thallium 201 &
Technetium 99 pyrophosphate.
Useful in pt. who can not exercise
Assessment of perfusion, infarction & ventricular
function
Hot spot technique(Tech-99) Infarcted
segment is detected as hot spot by gamma
camera
Cold spot technique-th201 taken by areas with
normal perfusion , cold spot represent area of
decreased perfusion

Coronary angiography
To situations where revascularization can
improve long-term survival- Unstable
coronary syndrome
Information about coronary artery and
presence and pattern of atherosclerotic
disease, specially suspected left main or
triple vessel diseases.
Intra cardiac pressure and cardiac output
Anatomy of cong. Heart disease.

Grading of Ejection fraction

55-75% -Normal contracting left
ventricle
40-55%-Decrese myocardial
contractalty Either due to previous MI
or increase afterload due to
hypertension- usually asymptomatic
25-40%- Pt symptomatic During
Exercise.
<25%- symptomatic at rest (NYHA
class IV)

Assessment of Left ventricular

Function

Good function
EF>55%
LVEDP<12 mm hg
Cardiac index> 2.5
ltr/min/m2
No area of
ventricular
dyskinesia

Impaired
Function
EF< 40%
LVEDP>18 mm hg
Cardiac index<
2ltr/min/m2
Multiple areas of
ventricular
dyskinesia

CONCLUSION

Thorough history,
Detailed physical examination,
Judicious use of tests.
Categorize patients into low,
intermediate & high risk
Combine preop assessment with
periop risk reduction strategies &
optimize medical treatment to
improve outcome.

THANK YOU